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326
M. Sakr
Treatment of children and adolescents with
1.3 μg/kg/day thyroxine for 24 months was
shown in a recent study to cause signicant
reduction in thyroid size in patients with autoimmune thyroiditis, but not affect antibody levels,
or signicantly alter TSH or freeT4 [261].
When L-T4 and seleno-methionine are given
together, they reduce the release of cytokines
from monocytes and lymphocytes thus reducing
the thyroid peroxidase antibody titre and autoimmune process in HT [262].
The additional role of diet for the management
of HT is usually overlooked, and careful supplementation of possible deciencies in HT is recommended for the dietary management of these
patients. There are specic nutrients that should
be regularly taken to maintain a healthy and functional thyroid. The top nutrients are Iodine (I2),
Selenium (Se), and Zinc (Zn). A diet optimizing
these nutrients is vital to an overall recovery plan.
Diets benecial for patients with HT include
paleo diet, gluten- free diet, and vegetarian or
vegan diet. Gluten and goitrogens are the worst
foods to have in diet of patients with HT as they
can have a negative impact on the thyroid.
Surgery
Surgery is generally avoided in HT as it is unnecessary to induce hypothyroidism. Thyroidectomy
is considered in patients with cosmetic problem,
with compressive symptoms (e.g., dysphagia,
dyspnea, and dysphonia), suspicion of malignancy as PTC is commonly associated. Surgery
has also benecial effect in cases of “painful thyroiditis” [263].
Radioactive Iodine (RAI)
RAI treatment can be considered as a “last
option” in elderly patients with large goiter in
whom thyroiditis is not responding to L-T4 and
refusing surgery [263].
Prognosis
With early diagnosis, timely institution of L-T4
replacement therapy, informed patient follow-up
care, and attention to other attendant complications, the prognosis in HT is excellent, with
patients leading a normal life.
Untreated “myxedema coma” has a poor prognosis and a high mortality rate. “Transient periods of thyrotoxicosis” sometimes occur, and
rarely the illness may progress to full hyperthyroid
Graves’ disease with active orbitopathy (bulging,
inamed eyes). The increased prevalence of
“lipid disorders” in association with untreated
hypothyroidism has the potential to increase
morbidity from coronary artery disease.
The risk for “PTC” is increased in patients
with HT, though not clearly more aggressive than
other PTCs [264]. Primary thyroid “B- cell lym-
phoma” affects <1/1000 patients, and it is more
likely to affect those with long-standing autoimmune thyroiditis.
Complications of over-replacement with L-T4
include accelerated bone loss, reduction in bone
mineral density, osteoporosis, tachycardia,
increased cardiac wall thickness, and contractility, which raise the risk of cardiac arrhythmias
(especially atrial brillation), particularly in the
elderly.
12.5.15.2 Focal Lymphocytic
Thyroiditis (Focal
Autoimmune Thyroiditis)
This low-grade autoimmune thyroiditis is characterized by focal lymphocytic inltrates of <5% of
the thyroid gland and is found coincidentally in
50% of women’s and 25% of men’s autopsies,
without clinical relevance.
12.5.15.3 Postpartum Thyroiditis
Postpartum thyroiditis occurs in 2–16% of
women within 6–12 months after delivery (or
abortion) [265, 266]. It represents an exacerbation of a preceding (undiagnosed) autoimmune
thyroiditis and is classically linked to the haplotypes HLA-DR3, -DR4, and -DR5. Most patients
(85%) develop autoantibodies against TPO and
Tg, which may disappear with time. Women with
a known autoimmune thyroiditis prior to pregnancy and an elevated titer of autoantibodies
against Tg during pregnancy nearly always suffer
from a postpartum exacerbation of their autoimmune thyroiditis. Clinically, patients may show a
transient hyperthyroidism state, which rapidly
converts to hypothyroidism, and then to euthy-
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12 Benign Thyroid Disease
327
roidism within 12months. Treatment consists of
thyroid hormone replacement when required.
12.5.15.4 Subacute de Quervain’s
Thyroiditis
Synonyms include granulomatous, pseudotuberculous, or giant cell, thyroiditis. Subacute de
Quervain’s thyroiditis is a self-limiting disease
accounting for 0.5–3% of all thyroid diseases and
lasts for up to 2 months [267]. A post-viral
cytokine- mediated inammation of the thyroid is
suspected because of the seasonal frequency and
association with upper respiratory tract infection.
In 50% of patients, antibodies against mumps,
measles, inuenza, adenovirus, Coxsackie virus,
or echovirus are found. Furthermore, a genetic
predisposition exists with the haplotype
HLA-Bw35.
Women are three to six times more affected
than men, with a peak incidence between the second and fth decades of life. Symptoms include
pain in the neck that irradiates to the jaw, ear,
face, and down to the chest, fever, lassitude, and
weakness. Physical examination reveals an
exquisitely tender and enlarged gland. The erythrocyte sedimentation rate (ESR) is markedly elevated. Initially, there is transient hyperthyroidism
from destruction of the thyroid follicles by the
local inammation process. Later on, hypothyroidism emerges due to inability to cope with the
body’s demand for thyroid hormones, and nally,
as healing occurs, euthyroidism is restored.
However, permanent hypothyroidism requiring
replacement therapy may occur in 15% of
patients, and recurrence may be noted in,
although at a low rate of 4% [268].
Subacute should be differentiated from acute
suppurative thyroiditis. In de Quervain’s thyroiditis, the gland sonographically reveals irregular
hypo-perfused areas instead of hyper-perfused
tissue seen with acute suppurative thyroiditis. On
FNA, the differential diagnosis further includes
palpation thyroiditis, in addition to other granulomatous diseases such as sarcoidosis, tuberculosis
(TB), and rheumatoid diseases.
Treatment is supportive with nonsteroidal
anti-inammatory drugs (NSADs) and β-blockers
in severe cases with hyperthyroidism.
Corticosteroids are useful when the NSAD medication is not successful, and symptoms usually
improve within 2–3 days after the initiation of
treatment. However, it may take about 4 weeks
for the disappearance of the thyroid mass.
12.5.15.5 Silent (Painless) Thyroiditis
(Subacute Lymphocytic
Thyroiditis)
Patients with painless thyroiditis present with a
diffuse but mild enlargement of the thyroid gland.
Thyroid function tests reveal a transient hyperthyroidism, followed by hypothyroidism and,
nally, return to euthyroidism. Autoantibodies
against TPO and Tg are found, as well as an association with HLA-DR3 and -DR5 haplotypes.
Histological examination reveals lymphocytic
inltration with destruction of follicles (in contrast to HT) and absence of giant cell granulomas
(in contrast to subacute thyroiditis). Women are
more often affected than men with a peak of incidence in middle life and the postpartum period. It
is a self-limited disease and rarely necessitates
thyroid replacement therapy.
A signicant percentage of patients with silent
thyroiditis have personal or family history of
autoimmune thyroid disease. Most patients have
a complete remission, but some develop persistent hypothyroidism. Some patients have had
alternating episodes of typical “high-uptake” thyrotoxicosis and episodes of “transient” lowuptake thyrotoxicosis [269]. Recurrence of
disease is common in silent thyroiditis but very
rare in subacute thyroiditis.
12.5.15.6 Riedel’s Fibrosing Thyroiditis
Riedel’s thyroiditis is a rare chronic thyroiditis in
which the thyroid gland is replaced by brous tissue. The underlying etiologic mechanisms are
unclear, though an autoimmune relation is suspected, due to elevated titers of thyroid autoantibodies. It is generally considered as a part of a
multifocal bro-inammatory process also
involving other tissues such as the mediastinum,
liver, lung, retro-peritoneum, and orbit.
Women in middle to advanced ages are more
affected than men. The clinical often resembles
malignancy due to the hard consistency of the
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M. Sakr
gland. Patients usually complain of rapid indolent enlargement of the thyroid that becomes very
hard and may suffer from neck discomfort, dysphagia, hoarseness of voice, and hypoparathyroidism (due to involvement of the RLN and
parathyroid glands). Approximately, 30–40% of
patients develop overt hypothyroidism. Physical
examination, laboratory analysis, cytology, and
imaging features are not useful for differentiating
between Riedel’s thyroiditis and neoplastic diseases or the brotic variant of Hashimoto’s thyroiditis [270].
Histological examination is necessary to
establish the nal diagnosis, and so surgical
biopsy is mandatory. The differential diagnosis
further includes anaplastic carcinoma and sarcoma of the thyroid. In contrast to the brotic
variant of Hashimoto’s thyroiditis where brosis
is strictly limited to the gland, Riedel’s thyroiditis
displays a dense brotic replacement of thyroid
parenchyma that penetrates the capsule and
extends into contiguous neck structures. Once the
diagnosis is conrmed, treatment is supportive
with thyroid hormone replacement when
required.
12.5.16 Non-autoimmune Thyroiditis
Nonimmune thyroiditis consists of a heterogeneous and rare group of thyroid inammatory
diseases. Some of them are infectious while others are clearly iatrogenic, such as drug-induced
thyroiditis and post-operative necrotizing
thyroiditis.
12.5.16.1 Acute Infectious Thyroiditis
(Acute Suppurative
Thyroiditis)
Infectious thyroiditis is a rare disease of the thyroid gland caused by bacterial or fungal infection, though mycobacterial, parasitic, and viral
forms of thyroiditis have also been described,
particularly in immune-suppressed individuals.
The thyroid gland appears to be relatively resistant to infection. The protective mechanisms
include a rich vascular supply, extended lymphatic drainage, a brous capsule, fascial planes
that anatomically separate the thyroid from
other cervical structures, and the high iodine
content of the gland, which may have a bactericidal effect. Infection of the gland occurs, either
through hematogenous spread from a primary
focus or by direct extension from adjacent neck
structures, especially in children [271]. Other
less common sources of infection include neck
trauma, lymphatic spread, or rarely, surgical site
infections [272]. The most common predisposing factor for suppurative thyroiditis is immunosuppression associated with HIV, TB, old age,
or debilitating diseases. Other predisposing factors include preexisting thyroid diseases, such
as MNG, autoimmune thyroiditis, and cancer
[272–274].
Patients usually present with fever and a painful, mostly unilateral, enlargement of the thyroid,
and local inammatory signs. Thyroid function
tests are usually normal, but a slight hyper- or
hypothyroidism may occur. Laboratory tests
show leucocytosis and elevated ESR. Neck US
shows patchy hyper-perfused areas in the thyroid
with liquid content (pus) when an abscess is present. A FNAC and cultures can identify the pathogen and guide the anti-microbial treatment.
Immuno-suppressed patients tend to present with
more chronic thyroid infections, bilateral disease,
and less prominent signs and symptoms.
Diagnosis may be reached with a high index of
suspicion and aspiration biopsy.
The differential diagnosis includes de
Quervain’s thyroiditis, hemorrhage into a thyroid
nodule, infected thyroglossal or branchial cyst,
infected cystic hygroma, and cervical lymphadenitis. In addition to FNA, US helps to establish
the diagnosis, which may further be rened by
CT scan.
When an abscess is identied, surgical drainage is essential. Occasionally, complete resection
of an affected lobe is required. In patients with
recurrent acute thyroiditis, an undetected stula
must be postulated. Complete removal of the
infected stula is, therefore, required to prevent
recurrence. Injection of 0.5% methylene blue
solution through a Nélaton’s catheter into the stula usually enables the complete resection of the
tract. When the origin of the stula is difcult to
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12 Benign Thyroid Disease
329
identify, transection of the inferior pharyngeal
constrictor muscle makes intervention easier.
12.5.16.2 Drug-Induced Thyroiditis
Certain drugs have been reported to cause thyroiditis, such as chronic I2 therapy, long-term
lithium therapy, and anti-convulsants (e.g., phenytoin and carbamazepine [216]). Moreover,
patients with chronic hepatitis or cancer treated
with interferon (IFN)-α will develop painless
thyroiditis in about 1–5% of cases [275].
Elevated anti-thyroid antibodies are noted in a
higher percentage of these patients, and permanent hypothyroidism or Graves’ disease may
appear. Thus, TSH should be measured prior to
initiation of IFN-α therapy and periodically during treatment [276].
A painless thyroiditis has been reported in
about 2% of the patients treated with Interleukin-2
(IL-2), which is used for immune-modulation in
malignant melanoma, renal cell carcinoma, and
leukemia, alone or in combination with chemotherapy. Finally, the anti-arrhythmic drug amiodarone contains 35% I2 and may cause a thyrotoxic
crisis or conversely, cause hypothyroidism.
Amiodarone decreases the conversion of T4 to
the biologically active T3. If amiodarone therapy
is topped, it is not eliminated for months due to
its very long half-life [277].
12.5.16.3 Postoperative Necrotizing
Thyroiditis
Postoperative necrotizing thyroiditis is a rare surgical complication owing to the very rich vascular supply of the thyroid [278, 279]. It is related
to glandular trauma by vigorous manipulation at
surgery or through repeated FNA [280]. Such
manipulation could induce an acute thyroiditis,
which in turn may lead to thyrotoxicosis or necrotizing thyroiditis. No predictive marker or factor has been identied. Histologically, the
specimen typically shows postoperative granulomas, as found in other organs (bladder, prostate)
following surgery.
12.5.16.4 Radiation Thyroiditis
Radiation thyroiditis occurs in a dose-related
fashion after RAI or external beam radiation ther-
apy, which causes follicle destruction resulting in
a transient hyperthyroidism, followed eventually
by hypothyroidism. Neck pain and tenderness
usually develop 5–10days following treatment.
Symptoms are mild and subside spontaneously in
a week.
12.5.16.5 Other Causes ofNonImmune
Thyroiditis
Other causes of thyroiditis are related to a local
process, such as an acute hemorrhage into a thyroid cyst or nodule. “Palpation thyroiditis” refers
to mild, self-limited thyroiditis occurring after
physical examination, surgery, or trauma to the
thyroid. It is not associated with any thyroid disease. Finally, thyroiditis may be caused by systemic diseases, such as vasculitis-associated
thyroiditis (phenytoin therapy), sarcoidosis, metastatic cancer, or a globus hystericus [281].
12.5.17 Indications ofSurgery
inThyroiditis
Surgical interventions are exceptionally indicated for the management of thyroiditis, accounting for <1% of all thyroid procedures [282].
Patients with “autoimmune thyroiditis” are effectively managed with thyroid hormone replacement therapy, and surgical treatment is the
exception. Technical difculties are encountered
by the surgeon as the glands are rm, rigid, and
highly vascular and the surrounding tissues are
inamed with lymphadenopathy, rendering the
parathyroids and RLNs at risk. In the rare instance
where a large HT may develop and become
symptomatic, TT is an option [219, 282, 283].
Moreover, as thyroiditis patients bear a higher
risk of developing thyroid carcinoma, a cold nodule suspicious on FNA may indicate a thyroid
lobectomy. Similarly, the rapid growth of a
chronic lymphocytic thyroid gland is suggestive
of NHL.While TT may surgically cure a stage I
lymphoma (conned to the thyroid), most thyroid
lymphomas involve regional LNs and distant
sites and require multi-modal systemic therapy.
Open biopsy or thyroid lobectomy is sufcient in
these cases to establish the denitive diagnosis.
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M. Sakr
A subacute de Quervain’s thyroiditis exceptionally deserves thyroidectomy. This indication
is given when intractable neck pain is present in
spite of a consequent analgesic and L-thyroxin
replacement therapy over a period of 6months
[282]. The brotic variant of HT is characterized
by a rapid enlargement of a preexisting goiter
that causes suspicion of a thyroid cancer and consequently surgery. Riedel’s brosing thyroiditis
often requires an open biopsy to conrm the
diagnosis and rule out an anaplastic carcinoma,
or isthmectomy and/or lobectomy to decompress
the trachea and esophagus. However, thyroidectomy can be highly demanding because of the
dense brotic reaction extending beyond the thyroid, which puts the surrounding structures at risk
of injury. Amiodarone-induced thyrotoxicosis in
the setting of a rare patient with otherwise intractable arrhythmia is an indication for thyroidectomy. Finally, the acute suppurative thyroiditis is
a classic indication for surgical drainage followed
by antibiotic therapy, and rarely for lobectomy
when the suppurative process is necrotizing.
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